Physiological monitor

ABSTRACT

A patient monitor has multiple sensors adapted to attach to tissue sites of a living subject. The sensors generate sensor signals that are responsive to at least two wavelengths of optical radiation after attenuation by pulsatile blood within the tissue sites.

INCORPORATION BY REFERENCE TO ANY PRIORITY APPLICATIONS

Any and all applications for which a foreign or domestic priority claimis identified in the Application Data Sheet as filed with the presentapplication are incorporated by reference under 37 CFR 1.57 and made apart of this specification.

BACKGROUND

The measurement of oxygen delivery to the body and the correspondingoxygen consumption by its organs and tissues is vitally important tomedical practitioners in the diagnosis and treatment of various medicalconditions. Oxygen delivery, the transport of oxygen from theenvironment to organs and tissues, depends on the orchestration ofseveral interrelated physiologic systems. Oxygen uptake is determined bythe amount of oxygen entering the lung and the adequacy of gas exchangewithin the lung. This gas exchange is determined by the diffusion ofoxygen from the alveolar space to the blood of the pulmonarycapillaries. Oxygen is subsequently transported to all organs andtissues by blood circulation maintained by the action of the heart. Theavailability of oxygen to the organs and tissues is determined both bycardiac output and by the oxygen content in the blood. Oxygen content,in turn, is affected by the concentration of available hemoglobin andhemoglobin oxygen saturation. Oxygen consumption is related to oxygendelivery according to Fick's axiom, which states that oxygen consumptionin the peripheral tissues is equal to oxygen delivery via the airway.

Oxygen delivery and oxygen consumption can be estimated from a number ofmeasurable parameters. Because of the diagnostic impracticalities ofmeasuring oxygen uptake and cardiac output, oxygen delivery is typicallyassessed from the oxygen status of arterial blood alone, such asarterial oxygen partial pressure, P_(a)O₂, and arterial oxygensaturation, S_(a)O₂. P_(a)O₂ represents the relatively small amount ofoxygen dissolved in the blood plasma. S_(a)O₂ represents the much largeramount of oxygen chemically bound to the blood hemoglobin. Oxygenconsumption is typically assessed from the oxygen status of mixed venousblood, i.e. the oxygen saturation of blood from the pulmonary artery,S_(v)O₂, which is used to estimate the O₂ concentration of bloodreturning from all tissues and organs of the body. These parameters canbe measured by both invasive and non-invasive techniques, exceptS_(v)O₂, which requires an invasive measurement.

Invasive techniques include blood gas analysis using the in vitromeasurement of extracted arterial or venous blood, drawn with a syringeand needle or an intervascular catheter. Arterial blood is commonlyobtained by puncturing the brachial, radial or femoral artery. Venousblood can be obtained from an arm vein, but such a sample reflects onlylocal conditions. To obtain mixed venous blood, which represents thecomposite of all venous blood, a long catheter is typically passedthrough the right heart and into the main pulmonary artery from aperipheral vein. Extracted blood gas analysis utilizes blood gasmachines or oximeters. A blood gas machine measures the partial pressureof oxygen, PO₂, using a “Clark electrode” that detects the currentgenerated by oxygen diffusing to a sealed platinum electrode across agas permeable membrane. An oximeter measures the oxygen saturation,S_(v)O₂, of oxygenated and deoxygenated hemoglobin usingspectrophotometry techniques that detect the differential absorption ofparticular wavelengths of light by these blood components.

Invasive monitoring also includes the in vivo monitoring of blood gasvia a catheter sensor inserted into an artery or vein. Miniaturizationof the Clark electrode allows placement of the electrode in a catheterfor continuous measurement of PO₂. A fiber optic equipped catheterattached to an external oximeter allows continuous measurement of oxygensaturation. Because of risks inherent in catheterization and thepromotion of blood coagulation by certain sensors, these techniques aretypically only used when vitally indicated.

Non-invasive techniques include pulse oximetry, which allows thecontinuous in vivo measurement of arterial oxygen saturation and pulserate in conjunction with the generation of a photoplethsymographwaveform.

Measurements rely on sensors which are typically placed on the fingertipof an adult or the foot of an infant. Non-invasive techniques alsoinclude transcutaneous monitoring of PO₂, accomplished with theplacement of a heated Clark electrode against the skin surface. Thesenon-invasive oxygen status measurement techniques are described infurther detail below.

SUMMARY

Prior art invasive oxygen assessment techniques are inherently limited.Specifically, in vitro measurements, that is, blood extraction andsubsequent analysis in a blood gas machine or an oximeter, arenon-simultaneous and non-continuous. Further, in vivo measurementsthrough catheterization are not casual procedures and are to beparticularly avoided with respect to neonates. Prior art noninvasivetechniques are also limited. In particular, conventional pulse oximetersare restricted to measurement of arterial oxygen saturation at a singlepatient site. Also, transcutaneous monitoring is similarly restricted tothe measurement of an estimate of arterial partial pressure at a singlepatient site, among other limitations discussed further below.

The stereo pulse oximeter according to the present invention overcomesmany of the limitations of prior art oxygen status measurements. Theword “stereo” comes from the Greek word stereos, which means “solid” orthree-dimensional. For example, stereophonic systems use two or morechannels to more accurately reproduce sound. The stereo pulse oximeteris similarly multi-dimensional, providing simultaneous, continuous,multiple-site and multiple-parameter oxygen status and plethysmograph(photoplethysmograph) measurements. The stereo pulse oximeter provides abenefit in terms of cost and patient comfort and safety over invasiveoxygen status estimation techniques. The multi-dimensional aspects ofthis invention further provide oxygen status and plethysmographmeasurements not available from current noninvasive techniques. Inaddition, the stereo pulse oximeter allows the isolation of noiseartifacts, providing more accurate oxygen status and plethysmographmeasurements than available from conventional techniques. The result isimproved patient outcome based on a more accurate patient assessment andbetter management of patient care.

In one aspect of the stereo pulse oximeter, data from a single sensor isprocessed to advantageously provide continuous and simultaneousmultiple-parameter oxygen status and plethysmograph measurements from aparticular tissue site. This is in contrast to a conventional pulseoximeter that provides only arterial oxygen saturation data from atissue site. In particular a physiological monitor comprises a sensorinterface and a signal processor. The sensor interface is incommunication with a peripheral tissue site and has an output responsiveto light transmitted through the site. The signal processor is incommunication with the sensor interface output and provides a pluralityof parameters corresponding to the oxygen status of the site, theplethysmograph features of the site or both. The parameters comprise afirst value and a second value related to the peripheral tissue site. Inone embodiment, the first value is an arterial oxygen saturation and thesecond value is a venous oxygen saturation. In this embodiment, anotherparameter provided may be the difference between arterial oxygensaturation and venous oxygen saturation at the tissue site. The venousoxygen saturation is derived from an active pulse generated at the site.The signal processor output may further comprise a scattering indicatorcorresponding to the site, and the sensor interface may further comprisea pulser drive, which is responsive to the scattering indicator tocontrol the amplitude of the active pulse. One of the parameter valuesmay also be an indication of perfusion.

In another aspect of the stereo pulse oximeter, data from multiplesensors is processed to advantageously provide continuous andsimultaneous oxygen status measurements from several patient tissuesites. This is in contrast to a conventional pulse oximeter thatprocesses data from a single sensor to provide oxygen status at a singletissue site. In particular, a physiological monitor comprises aplurality of sensor interfaces each in communications with one of aplurality of peripheral tissue sites. Each of the sensor interfaces hasone of a plurality of outputs responsive to light transmitted through acorresponding one of the tissue sites. A signal processor is incommunication with the sensor interface outputs and has a processoroutput comprising a plurality of parameters corresponding to the oxygenstatus of the sites, the plethysmograph features of the sites or both.The parameters may comprise a first value relating to a first of theperipheral tissue sites and a second value relating to a second of theperipheral tissue sites. In one embodiment, the first value and thesecond value are arterial oxygen saturations. In another embodiment, thefirst value and the second value are plethysmograph waveform phases. Thephysiological monitor may further comprise a sensor attachable to eachof the tissue sites. This sensor comprises a plurality of emitters and aplurality of detectors, where at least one of the emitters and at leastone of the detectors is associated with each of the tissue sites. Thesensor also comprises a connector in communications with the sensorinterfaces. A plurality of signal paths are attached between theemitters and the detectors at one end of the sensor and the connector atthe other end of the sensor.

In yet another aspect of the stereo pulse oximeter, data from multiplesensors is processed to advantageously provide a continuous andsimultaneous comparison of the oxygen status between several tissuesites. A conventional oximeter, limited to measurements at a singletissue site, cannot provide these cross-site comparisons. In particulara physiological monitoring method comprises the steps of deriving areference parameter and a test parameter from oxygen status measuredfrom at least one of a plurality of peripheral tissue sites andcomparing that reference parameter to the test parameter so as todetermine a patient condition. The reference parameter may be a firstoxygen saturation value and the test parameter a second oxygensaturation value. In that case, the comparing step computes a deltaoxygen saturation value equal to the arithmetic difference between thefirst oxygen saturation value and the second oxygen saturation value. Inone embodiment, the reference parameter is an arterial oxygen saturationmeasured at a particular one the tissue sites and the test parameter isa venous oxygen saturation measured at that particular site. In anotherembodiment, the reference parameter is a first arterial oxygensaturation value at a first of the tissue sites, the test parameter is asecond arterial oxygen saturation value at a second of the tissue sites.In yet another embodiment, the reference parameter is a plethysmographfeature measured at a first of the sites, the test parameter is aplethysmograph feature measured at a second of the sites and themonitoring method comparison step determines the phase differencebetween plethysmographs at the first site and the second site. In afurther embodiment, the comparing step determines a relative amount ofdamping between plethysmographs at the first site and the second site.The multi-dimensional features of these embodiments of the stereo pulseoximeter can be advantageously applied to the diagnosis and managedmedical treatment of various medical conditions. Particularlyadvantageous applications of stereo pulse oximetry include oxygentitration during oxygen therapy, nitric oxide titration during therapyfor persistent pulmonary hypertension in neonates (PPHN), detection of apatent ductus arteriosis (PDA), and detection of an aortic coarctation.

BRIEF DESCRIPTION OF THE DRAWINGS

The present invention will be described in detail below in connectionwith the following drawing figures in which:

FIG. 1A is a top-level block diagram of a stereo pulse oximeteraccording to the present invention;

FIG. 1B shows a single-sensor alternative embodiment to FIG. 1A;

FIG. 2 is a block diagram of the stereo pulse oximeter sensor interface;

FIG. 3 is a graph illustrating the absorption of red and infraredwavelengths by both oxygenated and deoxygenated hemoglobin;

FIG. 4 is a graph showing the empirical relationship between the “redover infrared” ratio and arterial oxygen saturation;

FIG. 5 is a block diagram of the analog signal conditioning for thesensor interface;

FIG. 6 is a functional block diagram of the stereo pulse oximeter signalprocessing;

FIG. 7 is a functional block diagram of the front-end signal processing;

FIG. 8 is a graph depicting the frequency spectrum of an arterialintensity signal;

FIG. 9 is a graph depicting the frequency spectrum of a combinedarterial and venous intensity signal;

FIG. 10 is a functional block diagram of the saturation calculationsignal processing;

FIG. 11 is a graph illustrating a plethysmograph waveform;

FIG. 12 is a graph illustrating the absorption contribution of variousblood and tissue components;

FIG. 13 is a graph illustrating an intensity “plethysmograph” pulseoximetry waveform;

FIG. 14 is a functional block diagram of the plethysmograph featureextraction signal processing;

FIG. 15 is a functional block diagram of the multiple parameter signalprocessing;

FIG. 16A is an illustration of a single-site stereo pulse oximeterdisplay screen;

FIG. 16B is an illustration of a multi-site stereo pulse oximeterdisplay screen;

FIG. 17A is a graph depicting a family of constant power curves for theelectrical analog of constant oxygen consumption;

FIG. 17B is a graph depicting arterial and venous oxygen saturationversus fractional inspired oxygen;

FIG. 17C is a graph depicting arterial minus venous oxygen saturationversus fractional inspired oxygen;

FIG. 18 is a three-dimensional graph depicting a delta oxygen saturationsurface;

FIG. 19 is an illustration of a neonatal heart depicting a pulmonaryhypertension condition;

FIG. 20 is an illustration of a fetal heart depicting the ductusarteriosis; and

FIG. 21 is an illustration of a neonatal heart depicting a patent ductusarteriosis (PDA).

DETAILED DESCRIPTION Stereo Pulse Oximetry

FIG. 1A illustrates the multi-dimensional features of a stereo pulseoximeter 100 according to the present invention. Shown in FIG. 1A is anexemplary stereo pulse oximeter configuration in which a first sensor110 is attached to a neonate's left hand, a second sensor 120 isattached to one of the neonate's feet, and a third sensor 130 isattached to the neonate's right hand. In general, these sensors are usedto obtain oxygen status and photoplethysmograph measurements atperipheral sites, including a person's ears and face, such as the noseand regions of the mouth in addition to hands, feet and limbs, but notincluding internal sites such as internal organs and the brain.

Each sensor 110, 120, 130 provides a stream of data through acorresponding sensor interface 114, 124, 134 to the digital signalprocessor (DSP) 150. For example, the first sensor 110 is connected toan input 112 of the first sensor interface 114, and the output 118 ofthe first sensor interface 114 is attached to a first data channel input152 of the DSP 150. Similarly, the second sensor 120 provides data to asecond data channel input 154 and the third sensor 130 provides data toa third data channel input 158.

FIG. 1B illustrates an alternative embodiment of the separate sensors110, 120, 130 (FIG. 1A). A stereo sensor 140 has multiple branches 112,122, 132 each terminating in a sensor portion 114, 124, 134. Each sensorportion 114, 124, 134 has two light emitters and a light detector, asdescribed below, and is attachable to a separate patient site. Thus, thestereo sensor 140 advantageously provides a single sensor device havingmultiple light emitters and multiple light detectors for attachment tomultiple patient tissue sites. A combination of the stereo sensor 140and a single patient cable 142 advantageously allows a single connection144 at the stereo pulse oximeter 100 and a single connection 146 at thestereo sensor 140.

The DSP 150 can independently process each data channel input 152, 154,158 and provide outputs 162 typical of pulse oximetry outputs, such asarterial oxygen saturation, Sp_(a)O₂, the associated plethysmographwaveform and the derived pulse rate. In contrast with a conventionalpulse oximeter, however, these outputs 162 include simultaneousmeasurements at each of several patient tissue sites. That is, for theconfiguration of FIG. 1A, the stereo pulse oximeter 100 simultaneouslydisplays Sp_(a)O₂ and an associated plethysmograph waveform for threetissue sites in addition to the patient's pulse rate obtained from anyone of sites. Further, the DSP 150 can provide unique outputsunavailable from conventional pulse oximeters. These outputs 164 includevenous oxygen saturation, Sp_(v)O₂, a comparison of arterial and venousoxygen saturation, Δ_(sat)=Sp_(av)O₂=Sp_(a)O₂−Sp_(v)O₂, and pleth, whichdenotes plethysmograph shape parameters, for each site. In addition, theDSP 150 can provide cross-site outputs that are only available usingstereo pulse oximetry. These unique cross-site outputs 168 includeΔsat_(xy)=Sp_(ax)O₂−Sp_(ay)O₂, which denotes the arterial oxygensaturation at site x minus the arterial oxygen saturation at site y.Also included in these outputs 168 is Δpleth_(xy), which denotes acomparison of plethysmograph shape parameters measured at site x andsite y, as described in detail below. The stereo pulse oximeter alsoincludes a display 180 capable of showing the practitioner the oxygenstatus and plethysmograph parameters described above. The display 180has a multiple channel graphical and numerical display capability asdescribed in more detail below.

Pulse Oximetry Sensor

FIG. 2 depicts one stereo pulse oximeter data channel having a sensor110 and a sensor interface 114 providing a single data channel input 152to the DSP 150. The sensor 110 is used to measure the intensity of redand infrared light after transmission through a portion of the bodywhere blood flows close to the surface, such as a fingertip 202. Thesensor 110 has two light emitters, each of which may be, for example, alight-emitting diode (LED). A red emitter 212, which transmits lightcentered at a red wavelength and an infrared (IR) emitter 214, whichtransmits light centered at an infrared wavelength are placed adjacentto, and illuminate, a tissue site. A detector 218, which may be aphotodiode, is used to detect the intensity of the emitted light afterit passes through, and is partially absorbed by, the tissue site. Theemitters 212, 214 and detector 218 are secured to the tissue site, withthe emitters 212, 214 typically spaced on opposite sides of the tissuesite from the detector 218.

To distinguish between tissue absorption at the two wavelengths, the redemitter 212 and infrared emitter 214 are modulated so that only one isemitting light at a given time. In one embodiment, the red emitter 212is activated for a first quarter cycle and is off for the remainingthree-quarters cycle; the infrared emitter 214 is activated for a thirdquarter cycle and is off for the remaining three-quarters cycle. Thatis, the emitters 212, 214 are cycled on and off alternately, insequence, with each only active for a quarter cycle and with a quartercycle separating the active times. The detector 218 produces anelectrical signal corresponding to the red and infrared light energyattenuated from transmission through the patient tissue site 202.Because only a single detector 218 is used, it receives both the red andinfrared signals to form a time-division-multiplexed (TDM) signal. ThisTDM signal is coupled to the input 112 of the sensor interface 114. Oneof ordinary skill in the art will appreciate alternative activationsequences for the red emitter 212 and infrared emitter 214 within thescope of this invention, each of which provides a time multiplexedsignal from the detector 218 allowing separation of red and infraredsignals and determination and removal of ambient light levels indownstream signal processing.

To compute Sp_(a)O₂, pulse oximetry relies on the differential lightabsorption of oxygenated hemoglobin, HbO₂, and deoxygenated hemoglobin,Hb, to compute their respective concentrations in the arterial blood.This differential absorption is measured at the red and infraredwavelengths of the sensor 110. The relationship between arterial oxygensaturation and hemoglobin concentration can be expressed as:

$\begin{matrix}{{{Sp}_{a}O_{2}} = {100\frac{C_{{HbO}\; 2}}{C_{Hb} + C_{{HbO}\; 2}}}} & (1)\end{matrix}$

That is, arterial oxygen saturation is the percentage concentration ofoxygenated hemoglobin compared to the total concentration of oxygenatedhemoglobin and deoxygenated hemoglobin in the arterial blood. Sp_(a)O₂is actually a measure of the partial oxygen saturation of the hemoglobinbecause other hemoglobin derivatives, such as COHb and MetHb, are nottaken into consideration.

FIG. 3 shows a graph 300 of the optical absorption properties of HbO₂and Hb. The graph 300 has an x-axis 310 corresponding to wavelength anda y-axis 320 corresponding to hemoglobin absorption. An Hb curve 330shows the light absorption properties of deoxygenated hemoglobin. AnHbO₂ curve 340 shows the light absorption properties of oxygenatedhemoglobin. Pulse oximetry measurements are advantageously made at a redwavelength 350 corresponding to 660 nm and an infrared wavelength 360corresponding to 905 nm. This graph 300 shows that, at these wavelengths350, 360, deoxygenated hemoglobin absorbs more red light than oxygenatedhemoglobin, and, conversely, oxygenated hemoglobin absorbs more infraredlight than deoxygenated hemoglobin.

In addition to the differential absorption of hemoglobin derivatives,pulse oximetry relies on the pulsatile nature of arterial blood todifferentiate hemoglobin absorption from absorption of otherconstituents in the surrounding tissues. Light absorption betweensystole and diastole varies due to the blood volume change from theinflow and outflow of arterial blood at a peripheral tissue site. Thistissue site might also comprise skin, muscle, bone, venous blood, fat,pigment, etc., each of which absorbs light. It is assumed that thebackground absorption due to these surrounding tissues is invariant andcan be ignored. Thus, blood oxygen saturation measurements are basedupon a ratio of the time-varying or AC portion of the detected red andinfrared signals with respect to the time-invariant or DC portion. ThisAC/DC ratio normalizes the signals and accounts for variations in lightpathlengths through the measured tissue. Further, a ratio of thenormalized absorption at the red wavelength over the normalizedabsorption at the infrared wavelength is computed:

$\begin{matrix}{\frac{RD}{IR} = \frac{\left( \frac{{Red}_{A\; C}}{{Red}_{D\; C}} \right)}{\left( \frac{{IR}_{A\; C}}{{IR}_{D\; C}} \right)}} & (2)\end{matrix}$

where Red_(AC) and IR_(AC) are the root-mean-square (RMS) of thecorresponding time-varying signals. This “red-over-infrared,ratio-of-ratios” cancels the pulsatile signal. The desired Sp_(a)O₂measurement is then computed from this ratio.

FIG. 4 shows a graph 400 depicting the relationship between RD/IR andSp_(a)O₂. This relationship can be approximated from Beer-Lambert's Law,as outlined below. However, it is most accurately determined bystatistical regression of experimental measurements obtained from humanvolunteers and calibrated measurements of oxygen saturation. The resultcan be depicted as a curve 410, with measured values of RD/IR shown on ay-axis 420 and corresponding saturation values shown on an x-axis 430.In a pulse oximeter device, this empirical relationship can be stored ina read-only memory (ROM) look-up table so that Sp_(a)O₂ can be directlyread-out from input RD/IR measurements.

According to the Beer-Lambert law of absorption, the intensity of lighttransmitted through an absorbing medium is given by:

$\begin{matrix}{I = {I_{0}{\exp \left( {- {\sum\limits_{i = 1}^{N}{ɛ_{i\; \lambda}c_{i}x_{i}}}} \right)}}} & (3)\end{matrix}$

where I₀ is the intensity of the incident light, ε_(i,λ). is theabsorption coefficient of the i^(th) constituent at a particularwavelength λ, c_(i) is the concentration coefficient of the i^(th)constituent and x_(i) is the optical path length of the i^(th)constituent. As stated above, assuming the absorption contribution byall constituents but the arterial blood is constant, taking the naturallogarithm of both sides of equation (3) and removing time invariantterms yields:

ln(I)=−[ε_(HbO2,λ) C _(HbO2)+ε_(Hb,λ) C _(hb) ]X(t)   (4)

Measurements taken at both red and infrared wavelengths yield:

RD(t)=−[ε_(HbO2,RD) C _(HbO2)+ε_(hb,RD) C _(hb) ]x _(RD)(t)   (5)

IR(t)=−[ε_(HbO2,IR) C _(HbO2) +ε _(Hb,IR) C _(hb) ]x _(IR)(t)   (6)

Taking the ratio RD(t)/IR(t) and assuming x_(RD)(t)≈x_(IR)(t) yields:

RD/IR=[ε _(HbO2,RD) C _(HbO2)+ε_(Hb,RD) C _(Hb)]/[ε_(HbO2,IR) C_(HbO2)+ε_(Hb,IR) C _(hb)]  (7)

Assuming further that:

C _(HbO2) +C _(Hb)=1   (8)

then equation (1) can be solved in terms of RD/IR yielding a curvesimilar to the graph 400 of FIG. 4.

Sensor Interface

FIG. 2 also depicts the sensor interface 114 for one data channel. Aninterface input 112 from the sensor 110 is coupled to an analog signalconditioner 220. The analog signal conditioner 220 has an output 223coupled to an analog-to-digital converter (ADC) 230. The ADC output 118is coupled to the DSP 150. The analog signal conditioner also has a gaincontrol input 225 from the DSP 150. The functions of the analog signalconditioner 220 are explained in detail below. The ADC 230 functions todigitize the input signal 112 prior to further processing by the DSP150, as described below. The sensor interface 114 also has an emittercurrent control input 241 coupled to a digital-to-analog converter (DAC)240. The DSP provides control information to the DAC 240 via the controlinput 241 for a pair of emitter current drivers 250. One driver output252 couples to the red emitter 212 of the sensor 110, and another driveroutput 254 couples to the IR emitter 214 of the sensor 110.

FIG. 5 illustrates one embodiment of the analog signal conditioner 220.The analog signal conditioner 220 receives a composite intensity signal112 from the sensor detector 218 (FIG. 2) and then filters andconditions this signal prior to digitization. The embodiment shown has apreamplifier 510, a high pass filter 520, a programmable gain amplifier530 and a low pass filter 540. The low pass filter output 223 is coupledto the ADC 230 (FIG. 2). The preamplifier 510 converts the currentsignal 112 from the detector 218 (FIG. 2) to a corresponding amplifiedvoltage signal. The gain in the preamplifier 510 is selected in order toprevent ambient light in the signal 112 from saturating the preamplifier510 under normal operating conditions. The preamplifier output 512 iscoupled to the high pass filter 520, which removes the DC component ofthe detector signal 112. The corner frequency of the high pass filter520 is set well below the multiplexing frequency of the red and infraredemitters 212, 214 (FIG. 2). The high pass filter output 522 couples tothe programmable gain amplifier 530, which also accepts a programminginput 225 from the DSP 150 (FIG. 2). This gain is set at initializationor at sensor placement to compensate for variations from patient topatient. The programmable gain amplifier output 532 couples to alow-pass filter 540 to provide anti-aliasing prior to digitization.

As described above, pulse oximetry measurements rely on the existence ofa pulsatile signal. The natural heart beat provides a pulsatile signalthat allows measurement of arterial oxygen saturation. In the systemiccirculation, all arterial pulsations are damped before flow enters thecapillaries, and none are transmitted into the veins. Thus, there is noarterial pulse component in the venous blood and absorption caused byvenous blood is assumed canceled by the ratio-of-ratio operationdescribed above. Venous blood, being at a relatively low pressure, will“slosh back and forth” during routine patient motions, such asshivering, waving and tapping. This venous blood sloshing creates atime-varying signal that is considered “noise” and can easily overwhelmconventional ratio-based pulse oximeters. Advanced pulse oximetrytechniques allow measurement of Sp_(v)O₂ under these circumstances. Forexample, such advanced techniques are disclosed in U.S. Pat. No.5,632,272, which is assigned to the assignee of the current application.This measurement is only available during motion or other physiologicalevents causing a time-varying venous signal.

The venous blood may also have a pulsatile component at the respirationrate, which can be naturally induced or ventilator induced. In adults,the natural respiration rate is 10-15 beats per minute (bpm). Inneonates, this natural respiration rate is 30-60 bpm. The ventilatorinduced pulse rate depends on the ventilator frequency. If thisrespiration induced venous pulse is of sufficient magnitude, advancedpulse oximetry techniques, described below, allow measurement ofSp_(v)O₂.

A controlled physiological event, however, can be created that allowsfor a continuous measurement of venous oxygen saturation, independent ofmotion or respiration. U.S. Pat. No. 5,638,816, which is assigned to theassignee of the current application discloses a technique for inducingan intentional active perturbation of the blood volume of a patient, andis referred to as an “active pulse.” Because peripheral venous oxygensaturation, Sp_(v)O₂, is a desirable parameter for stereo pulse oximetryapplications, it is advantageous to provide for a continuous andcontrolled pulsatile venous signal.

FIG. 2 depicts an active pulse mechanism used in conjunction with apulse oximetry sensor. An active pulser 260 physically squeezes orotherwise perturbs a portion of patient tissue 270 in order toperiodically induce a “pulse” in the blood at the tissue site 202. Apulser drive 280 generates a periodic electrical signal to a transducer262 attached to the patient. The transducer 262 creates a mechanicalforce against the patient tissue 270. For example, the pulser 260 couldbe a solenoid type device with a plunger that presses against the fleshytissue to which it is attached. The DSP 150 provides pulse drive controlinformation to a digital to analog converter (DAC) 290 via the controlinput 291. The DAC output 292 is coupled to the pulser drive 280. Thisallows the processor to advantageously control the magnitude of theinduced pulse, which moderates scattering as described below. The pulser260 could be a pressure device as described above. Other pressuremechanisms, for example a pressure cuff, could be similarly utilized.Other methods, such as temperature fluctuations or other physiologicalchanges, which physiologically alter a fleshy medium of the body on aperiodic basis to modulate blood volume at a nearby tissue site couldalso be used. Regardless of the active pulse mechanism, this modulatedblood volume is radiated by a pulse oximeter sensor and the resultingsignal is processed by the signal processing apparatus described belowto yield Sp_(v)O₂.

Signal Processor

FIG. 6 illustrates the processing functions of the digital signalprocessor (DSP) 150 (FIG. 1A). Each data channel input 152, 154, 158(FIG. 1A) is operated on by one or more of the front-end processor 610,saturation calculator 620, plethysmograph feature extractor 630 andmultiple parameter processor 640 functions of the DSP 150. First, adigitized signal output from the ADC 230 (FIG. 2) is input 602 to thefront-end processor 610, which demultiplexes, filters, normalizes andfrequency transforms the signal, as described further below. A front-endoutput 612 provides a red signal spectrum and an IR signal spectrum foreach data channel as inputs to the saturation calculator 620. Anotherfront-end output 614 provides a demultiplexed, normalized IRplethysmograph for each data channel as an input to the featureextractor 630. The saturation calculator output 622 provides arterialand venous saturation data for each data channel as input to themultiple parameter processor 640. One feature extractor output 632provides data on various plethysmograph shape parameters for each datachannel as input into the multiple parameter processor 640. Anotherfeature extractor output 634, also coupled to multiple parameterprocessor 640, provides an indication of plethysmograph quality and actsas a threshold for determining whether to ignore portions of the inputsignal 602. The multiple parameter processor has a numerical output 642that provides same-channel Δsat parameters and cross-channel parameters,such as Δsat_(xy) or Δpleth_(xy) to a display 180 (FIG. 1A). The numericoutput 642 may also provide saturation and plethysmograph parametersdirectly from the saturation calculator 620 or the feature extractor 630without further processing other than data buffering. The multipleparameter processor also has a graphical output 644 that providesplethysmograph waveforms for each data channel in addition to graphics,depending on a particular application, the indicate the trend of thenumerical parameters described above.

Front-End Processor

FIG. 7 is a functional block diagram of the front-end processor 610 forthe stereo pulse oximeter. The digitized sensor output 118 (FIG. 2) isan input signal 602 to a demultiplexer 710, which separates the inputsignal 602 into a red signal 712 and an infrared signal 714. Theseparated red and infrared signals 712, 714 are each input to a filter720 to remove unwanted artifacts introduced by the demultiplexingoperation. In one embodiment, the filter 720 is afinite-impulse-response, low-pass filter that also “decimates” orreduces the sample rate of the red and infrared signals 712, 714. Thefiltered signals 722 are then each normalized by a series combination ofa log function 730 and bandpass filter 740. The normalized signals,RD(t), IR(t) 742 are coupled to a Fourier transform 750, which providesred frequency spectrum and infrared frequency spectrum outputs, RD(ω),IR(ω) 612. A demultiplexed infrared signal output 614 is also provided.

Saturation Calculator

FIG. 8 shows a graph 800 illustrating idealized spectrums of RD(t) andIR(t) 752 (FIG. 7). The graph has an x-axis 810 that corresponds to thefrequency of spectral components in these signals and a y-axis 820 thatcorresponds to the magnitude of the spectral components. The spectralcomponents are the frequency content of RD(t) and IR(t), which areplethysmograph signals corresponding to the patient's pulsatile bloodflow, as described below. Thus, the frequencies shown along the x-axis810, i.e. f₀, f₁, f₂, are the fundamental and harmonics of the patient'spulse rate. The spectrum of RD(t), denoted RD(ω) 612 (FIG. 7), is shownas a series of peaks, comprising a first peak 832 at a fundamentalfrequency, f₀, a second peak 842 at a first harmonic, f₁ and a thirdpeak 852 at a second harmonic, f₂. Similarly, the spectrum of IR(t),denoted IR(ω) 612 (FIG. 7), is shown as another series of peaks,comprising a first peak 834 at a fundamental frequency, f₀, a secondpeak 844 at a first harmonic, f₁ and a third peak 854 at a secondharmonic, f₂. Also shown in FIG. 8 is the ratio of the spectral peaks ofRD(t) and IR(t), denoted RD(ω)/IR(ω). This ratio is shown as a firstratio line 838 at the fundamental frequency f₀, a second ratio line 848at the first harmonic f₁, and a third ratio line 858 at the secondharmonic f₂.

The magnitude of these ratio lines RD(ω)/IR(ω) corresponds to the ratioRD/IR defined by equation (2), and, hence, can be used to determineSp_(a)O₂. This can be seen from Parseval's relation for a periodicsignal, x(t), having a period T, where X_(k) is the spectral componentat the kth harmonic of x(t):

$\begin{matrix}{{\frac{1}{T}{\int_{0}^{T}{\left( {{x(t)}} \right)^{2}{dt}}}} = {\sum\limits_{k}\left( {X_{k}} \right)^{2}}} & (9)\end{matrix}$

Equation (9) relates the energy in one period of the signal x(t) to thesum of the squared magnitudes of the spectral components. The term|X_(k)|² can be interpreted as that part of the energy per periodcontributed by the kth harmonic. In an ideal measurement, the red andinfrared signals are the same to within a constant scale factor, whichcorresponds to the arterial oxygen saturation. Likewise, the red andinfrared spectra are also the same to within a constant scale factor.Thus, in an ideal measurement, all of the ratio lines 838, 848, 858 havesubstantially the same amplitude. Any differences in the amplitude ofthe ratio lines is likely due to motion, scattering or other noisecontaminations, as discussed further below. Accordingly, any of theRD(ω)/IR(ω) ratio lines is equivalent to the ratio, RD/IR, of equation(2) and can be used to derive Sp_(a)O₂.

One skilled in the art will recognize that the representations in FIG. 8are idealized. In particular, in actual measured data, especially ifcontaminated by noise, the frequencies of the peaks of RD(ω) do notcorrespond exactly to the frequencies of the peaks of IR(ω). Forexample, the fundamental frequency, f₀, found for RD(ω) will often bedifferent from the fundamental frequency, f₀', found for IR(ω) andsimilarly for the harmonics of f₀.

FIG. 9 shows a graph 900 illustrating idealized spectrums RD(ω) andIR(ω) and associated ratio lines measured with an active pulse sensor.The graph 900 has an x-axis 910 that corresponds to the frequency ofspectral components in these signals and a y-axis 920 that correspondsto the magnitude of the spectral components. The spectrum, RD(ω) , isshown as two series of peaks. One series of peaks 930 occurs at afundamental frequency, f_(h0), and associated harmonics, f_(h1) andf_(h2), of the patient's pulse (heart) rate. Another series of peaks 940occurs at a fundamental frequency, f_(p0), and associated harmonics,f_(p1) and f_(p2), of the active pulse rate. Similarly, the spectrum,IR(ω), is shown as two series of peaks. One series of peaks 950 occursat a fundamental frequency, f_(h0), and associated harmonics, f_(h1) andf_(h2), of the patient's pulse rate. Another series of peaks 960 occursat a fundamental frequency, f_(p0), and associated harmonics, f_(p1) andf_(p2), of the active pulse rate. Accordingly, there are two series ofRD/IR ratio lines. One series of ratio lines 970 are at the patient'spulse rate and associated harmonics, and another series of ratio lines980 are at the active pulser rate and associated harmonics.

Because only the arterial blood is pulsatile at the patient's pulserate, the ratio lines 970 are only a function of the arterial oxygensaturation. Accordingly, Sp_(a)O₂ can be derived from the magnitude ofthese ratio lines 970, as described above. Further, a modulation levelfor the active pulse is selected which insignificantly perturbates thearterial blood while providing a measurable venous signal. This ispossible because the arterial blood pressure is significantly largerthan the venous pressure. The modulation level is regulated as describedabove with respect to FIG. 2, i.e. the DSP 150, via a pulser drivecontrol 291, sets the magnitude of the pulser drive 280 to the pulseinducing mechanism 262. Assuming that the active pulse modulation of thearterial blood is insignificant, only the venous blood is pulsatile atthe active pulser rate. Hence, the ratio lines 980 are only a functionof the venous oxygen saturation. Accordingly, Sp_(a)O₂ can be derivedfrom the magnitude of the pulse rate related ratio lines 980 in the samemanner as Sp_(a)O₂ is derived from the magnitude of the pulse raterelated ratio lines.

Scattering

Propagation of optical radiation through tissue is affected byabsorption and scattering processes. The operation of pulse oximeterswas described qualitatively above using an analysis based on theBeer-Lambert law of absorption, equation (3). This approach, however,fails to account for the secondary effects of light scattering at pulseoximeter wavelengths. The primary light scatterer in blood iserythrocytes, i.e. red blood cells. A qualitative understanding of theeffects of scattering on pulse oximetry is aided by a description of redblood cell properties within flowing blood.

Human blood is a suspension of cells in an aqueous solution. Thecellular contents are essentially all red blood cells, with white cellsmaking up less the 1/600^(th) of the total cellular volume and plateletsless than 1/800^(th) of the total cellular volume. Normally thehematocrit, which is the percentage of the total volume of bloodoccupied by cells, is about 50% in large vessels and 25% in smallarterioles or venules.

Red blood cells are extremely deformable, taking on various shapes inresponse to the hydrodynamic stresses created by flowing blood. Forexample, assuming a laminar blood flow within a vessel, a parabolicvelocity profile exists that is greatest in the vessel center andsmallest along the vessel walls. Nominally, red blood cells are shapedas biconcave disks with a diameter of 7.6 um and thickness of 2.8 um.Exposed to this velocity profile, the red blood cells becomeparachute-shaped and aligned in the direction of the blood flow. Thus,during systole, transmitted light is scattered by aligned,parachute-shaped cells. During diastole, the light is scattered bybiconcave disks having a more or less random alignment.

The time-varying shape and alignment of the red blood cells can have asignificant effect on measured values of oxygen saturation if scatteringis ignored. Analogous to the analysis using the Beer-Lambert absorptionlaw, scattering can be qualitatively understood as a function of thescattering coefficients of various tissues. Specifically, the bulkscattering coefficient can be written as:

μ_(s) =V _(b)μ_(b) +V _(t)μ_(t)   (10)

where V_(b) is the blood volume, .μ_(b) is the scattering coefficient ofblood, V_(t) is the surrounding tissue volume and .μ_(t) is thescattering coefficient of the surrounding tissue. The volume, V_(t), andscattering coefficient, .μ_(t), of the surrounding tissue are timeinvariant. The blood volume, V_(b), however, is pulsatile. The ratio ofratios computation, RD/IR, results in normalization of the timeinvariant or DC tissue absorption and cancellation of the time varyingor AC pulsatile blood volume absorption to yield a number related tooxygen saturation. This computational approach is valid because theabsorption coefficients of blood, ε_(HbO2), λ, ε_(Hb, λ) given inequation (4) were assumed to change only slowly over time. Thescattering coefficient of blood .μ_(b), however, is time variant. Asdescribed above, this variation is due to the time-varying alignment andshape of the red blood cells. This time variation in the detectedintensity of light transmitted through a tissue site is not normalizedor canceled by the RD/IR calculation. Further, because the magnitude ofthe scattering coefficient variations is a function of blood flow, thesevariations become more pronounced with larger pulses in the bloodsupply. As a result, scattering produces frequency-dependent magnitudevariations in the ratio lines RD(ω)/IR(ω).

FIG. 9 illustrates the effect of scattering on the spectra of thedetected red and infrared intensity waveforms. When these waveforms aretransformed into the frequency domain, the time varying component ofscattering manifests itself as spreads 978, 988 in the RD/IR ratio linesat each harmonic of the plethysmograph or active pulse rate. Themagnitude of the ratio lines 970 at the fundamental and harmonics of thepatient's pulse rate varies between a minimum 972 and a maximum 974,resulting in a magnitude spread 978. Similarly, the magnitude of theratio lines 980 at the fundamental and harmonics of the active pulserate varies between a minimum 982 and a maximum 984, resulting in amagnitude spread 988. Normally, absent motion artifact or noisecontamination, the spread 978, 988 in the ratio lines is quiet small,but the magnitude of these spreads 978, 988, increases with larger bloodflows or pulse magnitudes. Scattering attributable to an active pulsecan be regulated by adjusting the magnitude of the active pulsemodulation based upon the amount of spread 978, 988 of the ratio linemagnitudes. Thus, the active pulse magnitude can be increased to obtaina larger detected AC signal, but limited to below the point at whichscattering becomes significant.

FIG. 10 depicts an embodiment of the signal processing for determiningoxygen saturation from the ratio lines of RD(ω)/RD(ω). The red spectrumRD(ω) 612 and infrared spectrum IR(ω) 612, computed as described abovewith respect to FIG. 7, are input to a peak detector 1010. The peakdetector 1010 separately calculates localized maximums for RD(ω) andIR(ω). The peak detector output 1012 is a series of frequenciescorresponding to the patient pulse rate fundamental and harmonics. If anactive pulse is used, the peak detector output 1012 is also a series offrequencies corresponding to the active pulse rate. Although the activepulse rate is known, the detected peaks may have been shifted due tonoise, motion artifact or other signal contamination. The peak detectoroutput 1012 is coupled to a series combination of peak matcher 1020 andratio line calculator 1030. The ratio lines RD/IR are calculated bymatching the frequency peaks of RD(ω) with the nearest frequency peaksof IR(ω). The ratio lines associated with the pulse rate harmonics 1032are then separated into a different set from the ratio lines associatedwith the active pulse harmonics 1034, assuming an active pulse isutilized. An average ratio line for each set 1032, 1034 is calculated byaveraging 1060 all ratio lines in a set. The magnitude of the averageratio line r 1062 for the pulse rate set 1032 is then fed to a look-uptable (LUT) 1090, which provides an output 622 of the measured value ofSp_(a)O₂. Similarly, if an active pulse is used, the magnitude of theaverage ratio line μ 1064 for the active pulse rate set 1034 is then fedto a LUT 1090, which provides an output 622 of the measured value ofSp_(v)O₂. A scattering detector 1080 computes the spread 988 (FIG. 9) inthe set of ratio lines associated with the active pulse and providesthis value 1082 to the DSP 150 (FIG. 2) so that the DSP can set thepulser drive control 291 (FIG. 2) to regulate the magnitude of theactive pulse.

Alternatively, Sp_(v)O₂ may be measured from respiration-induced pulsesin the venous blood, described above, without utilizing an active pulsesensor. Specifically, a series of ratio lines 980 (FIG. 9) would occurat a fundamental frequency, f_(r0), and associated harmonics, f_(r1) andf_(r2), of the respiration rate, which is either known from theventilator frequency or derived from a separate measurement of thenatural respiration. As shown in FIG. 10, the ratio lines associatedwith the respiration rate harmonics 1034 are then separated into adifferent set from the ratio lines associated with the pulse rateharmonics 1032. An average ratio line for the respiration rate set 1034is calculated by averaging 1060 all ratio lines in that set. Themagnitude of the average ratio lineμ 1064 for the respiration rate set1034 is then fed to a look-up table (LUT) 1090, which provides an output622 of the measured value of Sp_(v)O₂.

Plethysmograph Feature Extractor

FIG. 11 illustrates the standard plethysmograph waveform 1100, which canbe derived from a pulse oximeter. The waveform 1100 is a visualizationof blood volume change in the illuminated peripheral tissue caused byarterial blood flow, shown along the y-axis 1110, over time, shown alongthe x-axis 1120. The shape of the plethysmograph waveform 1100 is afunction of heart stroke volume, pressure gradient, arterial elasticityand peripheral resistance. The ideal waveform 1100 displays a broadperipheral flow curve, with a short, steep inflow phase 1130 followed bya 3 to 4 times longer outflow phase 1140. The inflow phase 1130 is theresult of tissue distention by the rapid blood volume inflow duringventricular systole. During the outflow phase 1140, blood flow continuesinto the vascular bed during diastole. The end diastolic baseline 1150indicates the minimum basal tissue perfusion. During the outflow phase1140 is a dicrotic notch 1160, the nature of which is disputed.Classically, the dicrotic notch 1160 is attributed to closure of theaortic valve at the end of ventricular systole. However, it may also bethe result of reflection from the periphery of an initial, fastpropagating, pressure pulse that occurs upon the opening of the aorticvalve and that precedes the arterial flow wave. A double dicrotic notchcan sometimes be observed, although its explanation is obscure, possiblythe result of reflections reaching the sensor at different times.

FIG. 12 is a graph 1200 illustrating the absorption of light at a tissuesite illuminated by a pulse oximetry sensor. The graph 1200 has a y-axis1210 representing the total amount of light absorbed the tissue site,with time shown along an x-axis 1220. The total absorption isrepresented by layers including the static absorption layers due totissue 1230, venous blood 1240 and a baseline of arterial blood 1250.Also shown is a variable absorption layer due to the pulse-added volumeof arterial blood 1260. The profile 1270 of the pulse-added arterialblood 1260 is seen as the plethysmograph waveform 1100 depicted in FIG.11.

FIG. 13 illustrates the photoplethysmograph intensity signal 1300detected by a pulse oximeter sensor. A pulse oximeter does not directlydetect absorption, and hence does not directly measure the standardplethysmograph waveform 1100 (FIG. 11). However, the standardplethysmograph can be derived by observing that the detected intensitysignal 1300 is merely an out of phase version of the absorption profile1270. That is, the peak detected intensity 1372 occurs at minimumabsorption 1272 (FIG. 12), and minimum detected intensity 1374 occurs atmaximum absorption 1274 (FIG. 12). Further, a rapid rise in absorption1276 (FIG. 12) during the inflow phase of the plethysmograph isreflected in a rapid decline 1376 in intensity, and the gradual decline1278 (FIG. 12) in absorption during the outflow phase of theplethysmograph is reflected in a gradual increase 1378 in detectedintensity.

FIG. 14 illustrates the digital signal processing for plethysmographfeature extraction 630 (FIG. 6). The input 614 is the IR signal outputfrom the demultiplexer 710 (FIG. 7). This signal is shifted into afirst-in, first-out (FIFO) buffer, which allows fixed-length portions ofthe input signal 614 to be processed for feature extraction. Thebuffered output signal 1412 is coupled to a shape detector 1420, slopecalculator 1430, feature width calculator 1440 and a notch locator 1450,which perform the core feature extraction functions. The shape detector1420 determines if a particular buffered signal portion 1412 containsspecific gross features, such as a peak, a valley, an upward slope, adownward slope, a dicrotic notch or a multiple dicrotic notch. Adetected shape output 1422 containing one or more flags indicating thegross feature content of the current signal portion 1412 is coupled tothe other feature extraction functions 1430, 1440, 1450 and to thewaveform quality determination functions 1460, 1470, 1480. A slopecalculator 1430 determines the amount of positive or negative slope inthe signal portion 1412 if the shape detector output 1422 indicates aslope is present. The output slope value 1432 is coupled to the waveformquality functions 1460, 1470, 1480 in addition to the feature extractionoutput 632. A feature calculator 1440 quantifies a feature in one ormore signal portions 1412 specified by the shape detector 1420, such asthe magnitude, the area under, or the width of a peak or notch. Thefeature calculator output 1442 is a code indicating the feature and itsvalue, which is coupled to the feature extraction output 632. A featurelocator 1450 quantifies the time of occurrence of one or more featuresof a signal portion 1412 as specified by the shape detector 1420. Thefeature locator output 1452, which is coupled to the feature extractionoutput 632, is a code indicating a feature and an associated codeindicating time of occurrence in reference to a particular epoch. Thefeature locator output 1452 allows a determination of the relativelocation of plethysmograph features in addition to a phase comparison ofplethysmographs derived from two or more tissue sites. Another featureextraction output 634, which is coupled to the multiple parameterprocessor 640 (FIG. 6), provides an indication of waveform quality.Input signals portions 1412 not having either a sharp downward edge1460, a symmetrical peak 1470 or a gradual decline 1480 are notprocessed further.

Multiple Parameter Processor

FIG. 15 illustrates the multiple parameter processing portion 640 (FIG.6) of the signal processing. A differencing function 1510 has as inputsa first saturation value, Sp₁O₂, and a second saturation value, Sp₂O₂,622. The saturation input values 622 can be arterial and venoussaturation values from a single data channel, arterial saturation valuesfrom two different data channels or venous saturation values from twodifferent data channels. The differences of the saturation value inputs622 are provided as an output 1514, which is coupled to a saturationdata memory 1520. The saturation values 622 are also directly coupled tothe saturation data memory 1520. The memory 1520 stores a record ofsaturation values, SpO₂, for each channel, delta saturation values,Δsat, for each channel and cross-channel delta saturation values,Δsat_(xy), as required for a particular application. A flow calculator1530 utilizes a plethysmograph input 614 or a bio-impedance probe input1534 to provide a flow value 1538, which is also coupled to thesaturation data memory 1520. For example, the flow value 1538 may be aperfusion index, PI, defined as follows:

$\begin{matrix}{{P\; I} = \frac{{IR}_{\max} - {IR}_{\min}}{{IR}_{D\; C}}} & (11)\end{matrix}$

where IR_(max) is the maximum value, IR_(min) is the minimum value, andIR_(DC) is the average value of the IR plethysmograph signal 614 (FIG.7).

The saturation data memory 1520 provides a buffered output 1522 that iscoupled to a numerical display driver 1540. The numerical display driver1540 provides an output 642 to a standard display, such as LED or LCDnumerical display modules or a CRT monitor. The memory output 1522 isalso coupled to a saturation data analyzer 1530, one function of whichcalculates a long-term trend of the values in memory 1520. For example,the saturation data analyzer may average a saturation value over time,or provide samples of the saturation values taken at regular timeintervals. The output 1532 can either be numerical, which is coupled tothe numerical display driver 1540, or graphical, which is coupled to thegraphical display driver 1570. The graphical display driver 1570provides an output 644 to a standard graphical display device, such asLED or LCD graphical display modules or a CRT monitor.

A pleth data memory 1550 has as inputs the IR plethysmograph signals 614(FIG. 7) from each data channel and the associated extracted features632 (FIG. 14). The memory 1550 also has an input indicating waveformquality 634 (FIG. 14). The pleth memory 1550 provides a buffered output1558 that is coupled to the graphical display driver 1570, allowingdisplay of the plethysmograph waveforms for each data channel. Thememory output 1558 is also coupled to a pleth data analyzer 1560, onefunction of which calculates a long-term trend of the plethysmograph andshape parameters in pleth memory 1520. For example, the pleth dataanalyzer 1560 may provide an average of particular shape parameters overtime. As another example, the pleth data analyzer 1560 may provide agraphic showing an accumulation of many overlaid plethysmographs. Theoutput 1562 can either be numerical, which is coupled to the numericaldisplay driver 1540, or graphical, which is coupled to the graphicaldisplay driver 1570.

Another function of the saturation data analyzer 1530 and the pleth dataanalyzer 1560 is to compare oxygen status and plethysmograph parametersderived from multiple sites in order to isolate noise artifacts and toderive a more accurate estimate of these parameters. For example, it isunlikely that motion artifact will affect each peripheral site in thesame manner. If the quality input 634 indicates a noisy plethysmographfor one channel during a particular time period, the pleth data analyzer1560 can exchange this information 1565 with the saturation dataanalyzer 1530. The saturation data analyzer 1530 can then ignore thesaturation data for that channel for that time period in lieu ofsaturation data from another channel. In a similar fashion, noisy datafrom multiple channels can be averaged, correlated or otherwiseprocessed to provide an estimate of Sp_(a)O₂, Sp_(v)O₂ or pulse rate, orto provide a plethysmograph that is more accurate than can be derivedfrom a single data channel.

FIG. 16A illustrates detail of a single-site display screen 180 for thestereo pulse oximeter. The display has a numerical display portion 1610controlled by the numerical display driver 1540 (FIG. 15) and agraphical display portion 1660 controlled by the graphical displaydriver 1570 (FIG. 15). The numerical display portion 1610 displays avalue for Sp_(a)O₂ 1620, Sp_(v)O₂ 1630 and pulse rate 1640 for aparticular tissue site. The graphical display portion 1660 displays aplethysmograph 1662 for the corresponding tissue site, which can bedisplayed as a single waveform or an accumulated multiple of overlayedwaveforms that may reveal a waveform trend. A push button or menuselection allows the user to switch to a display of data from any singleone of the multiple tissue sites to which a sensor is attached.

FIG. 16B illustrates detail of a multi-site display screen 180 for thestereo pulse oximeter. The numerical display portion 1610 displays avalue for Sp_(a)O₂ 1622 and Sp_(v)O₂ 1632 for a first tissue site. Alsodisplayed is a value for Sp_(a)O₂ 1624 and Sp_(v)O₂ 1634 for a secondtissue site. In addition, a value for pulse rate 1642 derived fromeither the first or second tissue site, or both, is displayed. Thegraphical display portion 1660 displays a first plethysmograph 1664 anda second plethysmograph 1666 corresponding to the first and secondtissue sites, respectively. A push button, menu selection allows theuser to manually switch between the single site display (FIG. 16A) andthe multi-site display (FIG. 16B). Also, a triggering event, such as analarm based on multiple-site oxygen status parameters, causes thedisplay to automatically switch from the single-site display to themulti-site display, enabling the user better view the conditions thatcaused the triggering event.

One of ordinary skill will appreciate many display screens variationsfrom those shown in FIGS. 16A and 16B that are within the scope of thisinvention. For example, the stereo pulse oximeter could be configured toprovide several push button or menu selectable display screens. Onedisplay screen might display more than two channels of oxygen statusdata. Another display screen could display cross-channel parameters suchas Δsat_(xy) or a comparison of plethysmograph shape parameters from twochannels. One of ordinary skill will also appreciate many variations andmodifications of layout and design for the graphical and numericaldisplays within the scope of this invention.

Stereo Pulse Oximetry Applications

Oxygen Titration

Oxygen is one of the most commonly used drugs in an intensive care unitand is an integral part of all respiratory support. The goal of oxygentherapy is to achieve adequate delivery of oxygen to the tissues withoutcreating oxygen toxicity. Too little oxygen results in organ damage and,in particular, brain damage. Too much oxygen can result in, for example,pulmonary edema and, in neonates, retinopathy of prematurity (ROP).Infants receiving oxygen therapy, in particular, must have inspiredoxygen concentration and blood oxygen levels monitored closely.

Oxygen titration in neonates is currently accomplished with eithertranscutaneous monitoring or monitoring with a conventional pulseoximeter. As mentioned above, transcutaneous monitoring involves theplacement of a heated Clark electrode against the skin surface. Theelectrode is secured to the skin surface with an airtight seal toeliminate contamination by room air gases. The skin surface beneath theelectrode is then heated, which opens pre-capillary sphincters allowinglocalized arteriolar blood flow beneath the sensor. The so-calledT_(c)O₂ value that is measured correlates well with P_(a)O₂. However,there are several drawbacks to this approach. Because the skin surfacemust be heated, a fifteen minute elapsed time after application isnecessary before stable readings are acquired. Further, the requiredtemperature is 43-45° C.(110° F.), with an associated risk of burns. Inaddition, titration is often accomplished by simply maintaining T_(c)O₂within acceptable limits for this parameter, e.g. an equivalent P_(a)O₂of 50-80 mm Hg for neonates. However, P_(a)O₂ alone does not provide anindication of balance between inspired oxygen and the rate of tissueoxygen consumption. If the patient is particularly anemic orhypovolemic, has an abnormal hemoglobin, or a small cardiac output, thenoxygen delivery may be inadequate even in the presence of a normalP_(a)O₂. Titration with a conventional pulse oximeter is similarlyaccomplished by maintaining Sp_(a)O₂ within acceptable limits, whichalso fails to consider tissue oxygen consumption.

Oxygen titration can be more adequately monitored with a continuousindication of oxygen consumption, which is equal to oxygen deliveryaccording to Fick's algorithm, as noted above. Further, continuousmonitoring of oxygen consumption at a peripheral tissue site, althoughnot necessarily indicative of overall oxygen consumption, may beindicative of an oxygen supply dependency. A measure of peripheraloxygen consumption can be expressed in terms of Δsat=Sp_(a)O₂-Sp_(v)O₂and perfusion, which, as noted above, are parameters advantageouslyprovided by the stereo pulse oximeter according to the presentinvention. Oxygen consumption at a peripheral site is obtained bymultiplying the difference between peripheral arterial and venous oxygencontent by perfusion at the site.

VpO₂=[O₂ content (arterial)−O₂ content (venous)]Φ  (12)

where oxygen content is measured in milliliters (ml) of O₂ perdeciliters (dl) of blood and Φ denotes perfusion in deciliters perminute. Oxygen content, however, can be expressed in terms of the amountof oxygen bound to the hemoglobin plus the amount of oxygen dissolved inthe plasma. The amount of bound oxygen is equal to the hemoglobinconcentration, C_(hb), in grams per deciliter of blood, times thehemoglobin carrying capacity, which is 1.34 milliliters of O₂ per gramof hemoglobin times the hemoglobin oxygen saturation, SO_(v)O₂. Theamount of dissolved oxygen is simply the partial pressure of oxygen,PO₂, times the O₂ solubility coefficient in blood, which is 0.003milliliters of O₂ per deciliter. The sum of these two terms yields:

O₂ content=1.34C _(Hb) SO₂+0.003PO₂   (13)

Substituting equation (13) into equation (12) yields the followingequation for tissue oxygen consumption:

VpO₂=[1.34C _(Hb)(Sp _(a)O₂ −Sp _(v)O₂)+0.003(P _(a)O₂ −P_(v)O₂)]Φ  (14)

Except when the fractional inspired oxygen, FiO₂, is high, blood plasmaplays a minimal role in oxygen delivery. Thus, peripheral oxygenconsumption is approximately:

VpO₂=[1.34C_(Hb)Δsat]Φ  (15)

In order to illustrate a schema of oxygen titration, it is convenient tocharacterize the relationship between oxygen supplied at the airway tooxygen consumed at a peripheral tissue site. Specifically,characterization of the relationship between Δsat, Φ and FiO₂ is useful.Assuming constant oxygen consumption at the tissue site, equation (15)is:

Δsat Φ=constant   (16)

Equation (16) has a simple analog in electronic circuits, i.e. avariable resistor across a current or voltage source adjusted tomaintain constant power. In this analog circuit, the current through theresistor, I, is equivalent to perfusion, the voltage across theresistor, V, is equivalent to Δsat and the constant of equation (16) isequivalent to the constant power, P, consumed by the resistor. Theequation representing this electrical analog is:

V×I=P   (17)

FIG. 17A shows a graph 1701 that depicts a family of curves eachcorresponding to different values of P in equation (17). The graph 1701has an x-axis 1710 indicating current, I, and a y-axis 1720 indicatingvoltage, V. A first curve 1730 shows V versus I for a constant power, P,of 0.5 watts; a second curve 1740 shows V versus I for a constant P of 1watt; and a third curve 1750 shows V versus I for a constant P of 2watts. Using the analogy between equations (16) and equation (17),whenever Φ (current) is small, the Δsat (voltage) is large andvice-a-versa. Also, a change in consumption (power) causes a shift inthe curve along with a change in its curvature. That is, if the bodysuddenly changes its metabolic rate at the peripheral tissue site, thecurve will accordingly shift up or shift down and will change its shape.Equation (16) and the analogous constant consumption curves of FIG. 17Aassume a supply independent condition, i.e. that peripheral oxygenconsumption is satisfied by peripheral oxygen delivery. If theperipheral tissue site is starved for oxygen, then the locus of pointsfor Δsat versus Φ is quite different from a hyperbola The amount oftissue oxygen extraction is at a maximum and is independent of Φ.Accordingly Δsat is at a maximum and independent of Φ. The aboveanalysis provides insight into the relationship between Δsat and Φ. Therelationship between Δsat and FiO₂ can also be characterized.

FIG. 17B shows a graph 1702 of saturation along a y-axis 1760 andfractional inspired oxygen along an x-axis 1770. A curve of Sp_(a)O₂1780 and a curve of Sp_(a)O₂ 1790 are depicted versus FiO₂. Thedifference between these curves 1780, 1790 yields Δsat 1785 versus FiO₂.When FiO₂ is zero 1772, oxygen saturation and, hence, both Sp_(a)O₂ 1780and Sp_(v)O₂ 1790 are zero. As FiO₂ is increased, Sp_(a)O₂ 1780 alsoincreases until virtually reaching 100 percent saturation 1762. As FiO₂increases further, Sp_(a)O₂ 1780 stays at virtually 100 percentsaturation 1762. As FiO₂ is increased from zero 1772, Sp_(v)O₂ 1790 alsoincreases. In this low FiO₂ region 1774, the peripheral tissue site issupply dependent and Δsat 1785 also increases. At a certain point, thetissue site oxygen demand is met by supply. In this supply independentregion 1776, oxygen consumption is constant and equation (16) is valid.Also, Δsat 1785 is at a constant maximum, which is a function of themetabolism at the tissue site. As FiO₂ increases further, eventually thepartial pressure of oxygen becomes significant and the second term ofequation (14) must be considered. In this high FiO₂ region 1778, Δsat1785 decreases because some of the tissue oxygen consumption is suppliedby oxygen dissolved in the plasma.

FIG. 17C shows a graph 1704 of saturation difference along a y-axis 1764and fractional inspired oxygen along an x-axis 1770. A curve of Δsat1786 is depicted versus FiO₂, corresponding to the region Δsat 1785depicted in FIG. 17B. The curve 1786 has a first deflection point 1766occurring at the transition between the low FiO₂ region 1774 (FIG. 17B)and the supply independent region 1776 (FIG. 17B). The curve 1786 alsohas a second deflection point 1768 occurring at the transition betweenthe supply independent region 1776 (FIG. 17B) and the high FiO₂ region1778 (FIG. 17B). The curve 1786 illustrates how the trend for Δsat, asmeasured by the stereo pulse oximeter, can be used to accurately titrateoxygen. The goal of oxygen titration is to supply sufficient oxygen tosupply tissue demand and avoid unnecessarily high amounts of FiO₂. Thus,the Δsat parameter should be monitored so that FiO₂ is adjusted betweenthe two deflection points 1766, 1768. For neonates, FiO₂ should beadjusted just beyond the first deflection point 1766. For adults, FiO₂should be adjusted just before the second deflection point 1768.

FIG. 18 illustrates a graph having a three-dimensional surface 1800generally depicting the relationship between Δsat,Φ and FiO₂ from thecombined graphs of FIGS. 17A and 17C. The graph has an x-axis 1810showing FiO₂, a y-axis 1820 showing Φ and a z-axis 1830 showing Δsat.The surface 1800 has a supply dependent region 1840, a perfusion-limitedregion 1850, a constant consumption region 1860 and a plasma dependentregion 1870. The surface describes the oxygen status of a peripheraltissue site. The supply dependent region 1840 corresponds to the lowFiO₂ region 1774 (FIG. 17B) described above. That is, inspired oxygeninto the lungs is so low that, at the tissue site, oxygen extraction bythe tissues is limited by oxygen delivery, and Δsat falls rapidly asFiO₂ is reduced. The perfusion-limited region 1850 along the x-axis 1810represents a low perfusion state where equation (16) is not valid. Thatis, perfusion at the tissue site is so low that oxygen extraction by thetissues is at a maximum, and, hence, Δsat is at a maximum and isindependent of FiO₂. A cross-section of the surface taken parallel tothe y-axis 1820 yields a hyperbole-shaped constant consumption region1860, consistent with the constant metabolic rate curves illustratedabove with respect to FIG. 17A. The plasma dependent region 1870corresponds to the high FiO₂ region 1778 (FIG. 17B) described above.That is, inspired oxygen into the lungs is so high that the tissue siteis partially dependent on oxygen dissolved in the plasma The surface1800 illustrates that perfusion should be monitored simultaneously withΔsat to avoid the perfusion-limited region 1850, where Δsat is anunresponsive indicator of FiO₂, and to avoid misinterpreting hyperbolicchanges in Δsat that result from changes in perfusion.

Persistent Pulmonary Hypertension in Neonates

FIG. 19 illustrates the heart/lung circulation of a hypertensiveneonate. Persistent Pulmonary Hypertension in Neonates (PPHN) is aneonatal condition with persistent elevation of pulmonary vascularresistance and pulmonary artery pressure. Shown is a neonatal heart 1902and a portion of a neonatal lung 1904. The pulmonary artery 1910 thatnormally feeds oxygen depleted “blue” blood from the right ventricle1920 to the lung 1904 is constricted. The back pressure from theconstricted artery 1910 results in a right-to-left shunting of thisoxygen depleted blood through the ductus arteriosus 1930, causing it tomix with oxygen rich “red” blood flowing through the descending aorta1940. PPHN treatment options include vasodilators, such as nitric oxide(NO). Inhaled exogenous NO causes a dose-dependent decrease in pulmonaryartery pressure and pulmonary vascular resistance, as well as a parallelincrease in pulmonary blood flow, without affecting systemic arterialpressure. However, the response to NO therapy is a function of the causeof the PPHN as well as the time elapsed before initiation of therapy.Potential toxic effects of NO dictate the proper titration of NO gas.Too little NO may not effectively relieve pulmonary hypertension, andtoo much NO may cause cellular injury or toxicity. NO therapy iscurrently monitored using intermittent ultrasound imaging and/or invitro blood gas measurements. The drawbacks to these techniques arenoncontinuous monitoring and disturbances to the neonate that canexacerbate or not reflect the hypertension in the non-disturbed state.

The stereo pulse oximeter according to the present invention allowsnoninvasive, continuous monitoring of a neonate for detection andmanaged treatment of PPHN that does not disturb the patient. A righthand sensor 130 (FIG. 1) provides arterial oxygen saturation and aplethysmograph for blood circulating from the left ventricle 1950through the innominate artery 1960, which supplies the right subclavianartery. Because the innominate artery 1960 is upstream from the shunt atthe ductus arteriosus 1930, the oxygen saturation value andplethysmograph waveform obtained from the right hand are relativelyunaffected by the shunt and serve as a baseline or reference forcomparison with readings from other tissue sites. Alternatively, areference sensor can be placed on a facial site, such as an ear, thenose or the lips. These sites provide arterial oxygen saturation and aplethysmograph for blood circulating from the left ventricle 1950 to theinnominate artery 1960, which supplies the right common carotid artery(not shown), or to the left common carotid artery 1965.

A foot sensor 120 (FIG. 1) provides oxygen status for blood suppliedfrom the descending aorta 1940. The shunt 1930 affects both the oxygensaturation and the blood flow in the descending aorta 1940. As statedabove, the shunt 1930 causes oxygen-depleted blood to be mixed withoxygen-rich blood in the descending aorta 1940. Because the descendingaorta 1940 supplies blood to the legs, the oxygen saturation readings atthe foot will be lowered accordingly. The PPHN condition, therefore, ismanifested as a higher arterial oxygen saturation at the right handreference site and a lower saturation at the foot site.

The shunt also allows a transitory left to right flow during systole,which distends the main pulmonary artery 1980 as the result of the bloodflow pressure at one end from the right ventricle and at the other endfrom the aortic arch 1990. A left-to-right flow through the shunt 1930into the distended artery 1980 alters the flow in the descending aorta1940 and, as a result, the plethysmograph features measured at the foot.The PPHN condition, therefore, also is manifested as a plethysmographwith a narrow peak and possibly a well-defined dicrotic notch at theleft hand baseline site and a broadened peak and possibly no notch atthe foot site.

An optional left hand sensor 110 (FIG. 1) provides oxygen status forblood circulating from the left ventricle through the left subclavianartery 1970 that supplies the left arm. Because the left subclavianartery 1970 is nearer the shunt 1930 than the further upstreaminnominate artery 1960, it may experience some mixing of deoxygenatedblood and an alteration in flow due to the shunt 1930. The PPHNcondition, therefore, may also be manifested as a reduced saturation andan altered plethysmograph waveform at the left hand site as comparedwith the right hand baseline site, although to a lesser degree than witha foot site. Thus, the PPHN condition can be detected and its treatmentmonitored from Δsat and plethysmograph morphology comparisons between aright hand baseline sensor site and one or more other sites, such as theleft hand or foot.

Patent Ductus Arteriosus

FIG. 20 illustrates the fetal heart/lung circulation. Shown is a fetalheart 2002 and a portion of a fetal lung 2004. The lung 2004 isnon-functional and fluid-filled. Instead, oxygenated blood is suppliedto the fetus from gas-exchange in the placenta with the mother's bloodsupply. Specifically, oxygenated blood flows from the placenta, throughthe umbilical vein 2006 and into the right atrium 2022. There, it flowsvia the foramen 2024 into the left atrium 2052, where it is pumped intothe left ventricle 2050 and then into the aortic trunk 2092. Also,oxygenated blood is pumped from the right atrium 2022 into the rightventricle 2020 and directly into the descending aorta 2040 via the mainpulmonary artery 2080 and the ductus arteriosus 2030. Normally, theductus arteriosus 2030 is only open (patent) during fetal life and thefirst 12 to 24 hours of life in term infants. The purpose of the ductusarteriosus 2030 is to shunt blood pumped by the right ventricle 2020past the constricted pulmonary circulation 2010 and into the aorta 2040.

FIG. 21 illustrates a neonatal heart 2002 with a patent ductusarteriosus 2030. The ductus arteriosus frequently fails to close inpremature infants, allowing left-to-right shunting, i.e. oxygenated“red” blood flows from the aorta 2040 to the now unconstricted pulmonaryartery 2010 and recirculates through the lungs 2004. A persistent patentductus arteriosus (PDA) results in pulmonary hyperperfusion and anenlarged right ventricle 2020, which leads to a variety of abnormalrespiratory, cardiac and genitourinary symptoms. Current PDA diagnosisinvolves physical examination, chest x-ray, blood gas analysis,echocardiogram, or a combination of the above. For example, large PDAsmay be associated with a soft, long, low-frequency murmur detectablewith a stethoscope. As another example, two-dimensional, color Dopplerechocardiography may show a retrograde flow from the ductus arteriosus2030 into the main pulmonary artery 2080. Once a problematic PDA isdetected, closure can be effected medically with indomethacin oribuprofen or surgically by ligation. Multiple doses of indomethacin arecommonplace but can still result in patency, demanding ligation. Adrawback to current diagnostic techniques is that clinical symptoms of aPDA can vary on an hourly basis, requiring extended and inherentlyintermittent testing.

The stereo pulse oximeter according to the present invention allows forcontinuous evaluation of PDA symptoms using non-invasive techniques. Aright hand sensor 130 (FIG. 1) provides arterial oxygen saturation and aplethysmograph for blood circulating from the left ventricle 2050through the innominate artery 2160, which supplies the right subclavianartery leading to the right arm. Because the innominate artery 2160 isupstream from the shunt at the ductus arteriosus 2030, the oxygensaturation value and plethysmograph waveform obtained from the righthand are relatively unaffected by the shunt and serve as a baseline forcomparison with readings from other tissue sites.

A foot sensor 120 (FIG. 1) provides oxygen status for blood suppliedfrom the descending aorta 2040. Unlike a PPHN condition, the shunt 2030does not affect oxygen saturation in the descending aorta 2040, becausethe relatively low pressure in the pulmonary artery 2010 does not allowa mixing of deoxygenated blood into the relatively high pressure flow ofoxygenated blood in the aorta 2040. However, like a PPHN condition, theshunt 2030 does affect the aortic flow. In particular, the shunt allowsa transitory left-to-right flow during systole from the high pressureaorta 2040 to the low pressure pulmonary circulation 2010. Thisleft-to-right flow through the shunt 1930 alters the flow in thedescending aorta 1940 and, as a result, the plethysmograph featuresmeasured at the foot. The PDA condition, therefore, is manifested as anormal plethysmograph with a characteristically narrow peak andwell-defined dicrotic notch at the right-hand baseline site comparedwith a damped plethysmograph with a broadened peak and reduced ormissing notch at the foot site. Further, the foot site waveform is phaseshifted from the baseline waveform. These plethysmograph differences areaccompanied by comparable arterial oxygen saturation values between theright-hand site and the foot site.

An optional left hand sensor 110 (FIG. 1) provides oxygen status forblood circulating from the left ventricle through the left subclavianartery 2170 that supplies the left arm. Because the left subclavianartery 2170 is nearer the shunt 2030 than the further upstreaminnominate artery 2160, it may experience some alteration in flow due tothe shunt 2030. The PDA condition, therefore, may also be manifested asan altered plethysmograph waveform at a left hand site as compared withthe right hand baseline site, although to a lesser degree than with afoot site. Thus, the PDA condition can be detected and its treatmentmonitored from Δsat_(xy)≈O and plethysmograph morphology and phasecomparisons between a right hand baseline sensor site and one or moreother sites, such as the left hand or foot. One of ordinary skill willrecognize that multiple site comparisons using the stereo pulse oximeterof the current invention may also be used to detect other cardiacabnormalities that cause mixing of oxygenated and deoxygenated blood,such as a ventricular hole or a patent foramen. Further, abnormal mixingof oxygenated and deoxygenated blood may also be manifested inmeasurements provided by the stereo oximeters other than Δsat_(xy) and.Δpleth_(xy) as described above. For example, an inversion in Δsat at aparticular tissue site, i.e., Sp_(v)O₂ being larger than Sp_(a)O₂ atthat site, would indicate such an abnormal condition.

Aortic Coarctation

Coarctation of the aorta is a congenital cardiac anomaly in whichobstruction or narrowing occurs in the distal aortic arch or proximaldescending aorta. It occurs as either an isolated lesion or coexistingwith a variety of other congenital cardiac anomalies, such as a PDA. Ifthe constriction is preductal, lower-trunk blood flow is suppliedpredominantly by the right ventricle via the ductus arteriosus, andcyanosis, i.e. poorly oxygenated blood, is present distal to thecoarctation. This can be detected by the stereo pulse oximeter from acomparison of Sp_(a)O₂ between an upper body and a lower body site. Ifthe constriction is postductal, blood supply to the lower trunk issupplied via the ascending aorta Differential plethysmographs betweenthe upper and lower extremities may not exist if the ductus is widelypatent. If the ductus closes, however, this condition can be detected bythe stereo pulse oximeter as a reduced amplitude and phase delay betweenthe plethysmographs measured at a lower body site with respect to anupper body site.

The stereo pulse oximeter has been disclosed in detail in connectionwith various embodiments of the present invention. These embodiments aredisclosed by way of examples only and are not to limit the scope of thepresent invention, which is defined by the claims that follow. One ofordinary skill in the art will appreciate many variations andmodifications within the scope of this invention.

What is claimed is:
 1. A physiological monitor comprising: interfacecomponentry in communication with at least two sensors each adapted tobe positioned at one of at least two peripheral tissue sites, saidinterface componentry having outputs corresponding to signals receivedfrom each of the at least two sensors and responsive to lighttransmitted through a corresponding one of said sites; and at least onesignal processor in communication with said interface componentryoutputs, said at least one signal processor receiving the outputs fromthe interface componentry and determining an indication of oxygensaturation values from said sites in response to the outputs, said atleast one signal processor further configured to compare at least onefirst oxygen saturation value from a first of said at least two siteswith at least one second oxygen saturation value from a second of saidat least two sites to determine the presence of a heart abnormality.